Effects of smoking cessation on β-cell function, insulin sensitivity, body weight, and appetite

Objective: To stop smoking is commonly associated with significant weight gain, but the mechanisms for this are poorly understood. We assessed the effects of smoking cessation on body weight, insulin sensitivity, beta-cell function, and appetite. Subjects and methods: Twenty-seven long-term smokers (n=27; nine females/18 males, 28 +/- 1 years, 22.9 +/- 0.6 kg/m(2)) attending an ambulatory smoking cessation program in a community hospital in Vienna, Austria were examined at baseline (Visit A; still smoking) and after a minimum of 3 months of smoking abstinence (Visit B; n=14); relapsed smokers were not followed up. Participants underwent 3-h oral glucose tolerance tests and body composition measurements at each study visit. Fasting (QUICKI) and dynamic (oral glucose insulin sensitivity (OGIS)) insulin sensitivity and beta-cell secretion (insulinogenic index 140 (IGI40)) were calculated. Food intake was quantified with a free choice buffet. Fasting plasma concentrations of neuropeptide-Y (NPY), peptide-YY (PYY), glucagon-like peptide 1 (GLP1), leptin, ghrelin, and visfatin were measured. Results: After >3 months' smoking abstinence, body weight, and fat mass were increased (+4 and +22% respectively, P<0.05) and fasting insulin sensitivity deteriorated (QUICKI: post, 0.37 +/- 0.02 vs baseline, 0.41 +/- 0.2; P<0.05), while OGIS remained unchanged throughout. IGI40 increased by 31% after >3 months' smoking abstinence (P<0.01). Carbohydrate ingestion increased after stopping smoking (P<0.05). NPY fasting levels were increased after >3 months (P<0.05), PYY, GLP1, leptin, ghrelin, and visfatin were unchanged. Conclusion: Smoking cessation is associated with transient metabolic changes including increased beta-cell secretion in response to glucose and fasting insulin resistance. These alterations may be associated with or contribute to the body weight gain after smoking cessation.